Skip to main content
. Author manuscript; available in PMC: 2014 Feb 1.
Published in final edited form as: Nat Immunol. 2013 Jun 30;14(8):812–820. doi: 10.1038/ni.2639

Figure 6. CD36 regulates NLRP3 activation by IAPP.

Figure 6

(a) Binding of FAM-conjugated human IAPP, (FAM-IAPP; 5-10 μM) and HiLyte-488-conjugated soluble Aβ (488-sAβ) to control (CHO-eV) or CD36-expressing CHO (CHO-CD36) cells. (b) Confocal microscopy of WT or Cd36–/– BMDM incubated with 10 μM soluble human IAPP for the indicated times or control rat IAPP for 24 h. Cells were fixed and stained with Alexa-568 conjugated cholera toxin B and thioflavin-S (Thio-S) to visualize intracellular amyloid. (c) Confocal microscopy of WT or Cd36–/– BMDM incubated with human IAPP (hIAPP) or soluble Aβ (sAβ, 10 μM, 24 h) and fluorescent Dextran-Red, then fixed and stained with thioflavin-S. Arrows indicate thioflavin-S-reactive amyloid. (d) IL-1β ELISA of supernatants from LPS primed WT, NLRP3-deficient (Nlrp3–/–) or Caspase-1 deficient (Ice–/–) BMDM treated for 6 h with vehicle (Ctrl) or huIAPP (10 μM). (e) IL-1β ELISA of supernatants from LPS primed WT or Cd36–/– BMDM treated for 6h with vehicle (Ctrl), hIAPP (10 μM) or control rat IAPP (rIAPP, 10 μM). (f) IL-β ELISA of supernatants from LPS-primed BMDM pre-treated with Congo Red (200 μM, 1 h) and incubated for 6 h with vehicle (Ctrl) or hIAPP (10 μM). Data in a, d-f are mean ± s.d. of triplicate samples within a single experiment and are representative of three independent experiments. Images in b-c are representative of three independent experiments. Scale bar = 10 μm. *P<0.05.